ArticleWorld journal of gastroenterology2009
Role of the receptor for advanced glycation end products in hepatic fibrosis.
Article in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- Preventive and Ameliorative Effects of Se- and Zn-Biofortified Chickpeas on MAFLD-Related Metabolic Disturbances.Foods (Basel, Switzerland) · 2026Article
- Personalized MASLD and liver fibrosis risk assessment for adults: glycemic status determines optimal choice of non-invasive indices.Diabetology & metabolic syndrome · 2025Article
- Curcumin mediates oxidative stress to play an anti-fibrotic role, focusing on liver, renal, myocardial and pulmonary fibrosis.Frontiers in pharmacology · 2025Review
- Article
- A standardized pomegranate fruit extract ameliorates thioacetamide-induced liver fibrosis in rats via AGE-RAGE-ROS signaling.Heliyon · 2023Article
- Increased Expression of S100B and RAGE in a Mouse Model of Bile Duct Ligation-induced Liver Fibrosis.Journal of Korean medical science · 2021Article
- AGER1 downregulation associates with fibrosis in nonalcoholic steatohepatitis and type 2 diabetes.The Journal of clinical investigation · 2020Article
- Advanced Glycation End Products as a Predictor of Diabetes Mellitus in Chronic Hepatitis C-Related Cirrhosis.Frontiers in medicine · 2020Article
- siRNA- and miRNA-based therapeutics for liver fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019Review
- High-Mobility Group Box-1 and Liver Disease.Hepatology communications · 2018Review
- Gene-disease associations identify a connectome with shared molecular pathways in human cholangiopathies.Hepatology (Baltimore, Md.) · 2018Article
- The Role of Glyoxalase-I (Glo-I), Advanced Glycation Endproducts (AGEs), and Their Receptor (RAGE) in Chronic Liver Disease and Hepatocellular Carcinoma (HCC).International journal of molecular sciences · 2017Review
- Increased liver AGEs induce hepatic injury mediated through an OST48 pathway.Scientific reports · 2017Article
- Ameliorative Effects of Nilotinib on CCl4 Induced Liver Fibrosis Via Attenuation of RAGE/HMGB1 Gene Expression and Oxidative Stress in Rat.Chonnam medical journal · 2017Article
- Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease.World journal of gastroenterology · 2016Article
- Small interfering RNA targeting receptor for advanced glycation end products suppresses the generation of proinflammatory cytokines.Experimental and therapeutic medicine · 2015Article
- Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies.World journal of hepatology · 2014Review
- Curcumin eliminates the effect of advanced glycation end-products (AGEs) on the divergent regulation of gene expression of receptors of AGEs by interrupting leptin signaling.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Classical and alternative activation of rat hepatic sinusoidal endothelial cells by inflammatory stimuli.Experimental and molecular pathology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the role of advanced glycation end products (AGE) and their specific receptor (RAGE) in the pathogenesis of liver fibrogenesis.
methodsIn vitro RAGE expression and extracellular matrix-related gene expression in both rat and human hepatic stellate cells (HSC) were measured after stimulation with the two RAGE ligands, advanced glycation end product-bovine serum albumin (AGE-BSA) and N(epsilon)-(carboxymethyl) lysine (CML)-BSA, or with tumor necrosis factor-alpha (TNF-alpha). In vivo RAGE expression was examined in models of hepatic fibrosis induced by bile duct ligation or thioacetamide. The effects of AGE-BSA and CML-BSA on HSC proliferation, signal transduction and profibrogenic gene expression were studied in vitro.
resultsIn hepatic fibrosis, RAGE expression was enhanced in activated HSC, and also in endothelial cells, inflammatory cells and activated bile duct epithelia. HSC expressed RAGE which was upregulated after stimulation with AGE-BSA, CML-BSA, and TNF-alpha. RAGE stimulation with AGE-BSA and CML-BSA did not alter HSC proliferation, apoptosis, fibrogenic signal transduction and fibrosis- or fibrolysis-related gene expression, except for marginal upregulation of procollagen alpha1(I) mRNA by AGE-BSA.
conclusionDespite upregulation of RAGE in activated HSC, RAGE stimulation by AGE does not alter their fibrogenic activation. Therefore, RAGE does not contribute directly to hepatic fibrogenesis.
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